Hemifacial spasm generally begins as involuntary muscle spasms in the eyelids and then progresses to the entire distribution of the facial nerve. This disease is thought to be due to a compression of the facial nerve at its root entry zone by one of several arteries in the region. The underlying neural mechanisms of the hemifacial spasm are still controversial. Arterial compression of the nerve can modify the facial nerve, facial motoneurons, and the trigeminal nucleus. This proposal investigates the role of each of these modifications in producing the symptoms of hemifacial spasm. Hemifacial spasm patients will used to identify changes in the trigeminal system. An animal model isolating the different mechanisms will be created to characterize the causes of symptom development resulting from motoneuron and trigeminal modifications.